The complexing of the p53 to the SV40 T antigen was studied in various cells. All p53 is in complex in almost all SV40 transformed murine fibroblast cells, however, in SV40 transformed Balb 3T12 cells most (Greater than 80%) of the p53 is free. This difference is not due to differences in the primary sequence of these two proteins, but correlates with a five times lower phosphorylation of the non-complexed protein species. SV40 transformed "immortalized" human placenta and amnion cells, which are epithelial and of throphoblast origin, contain only non-complexed p53. These findings pose the question to what extent, if any, the complexing with p53 is necessary for the transforming functions of the T antigen. In the developing mouse embryo during the second half of gestation the steady state level of p53 declines drastically, however, the p53 mRNA level seem to remain constant. This is in contrast to what occurs in cells stimulated to divide in culture, when there is a coordinated modulation of p53 and mRNA levels during the cell division cycle. The apparent translational modulation of p53 in embryogenesis is under study. We are working on a large family of highly tumorigenic mouse cell lines and clones (TD50=100) selected out from near normal (TD50=1.4 million) parental cloned fibroblasts by a single transplantation step. A very complex and interesting picture of transcriptional modulation is now emerging for numerous proto-oncogenes (and also for p53), but none which is qualitatively different between the normal parents and all the (mutant) tumorigenic progenies. The system is very useful to study the multifarious molecular possibilities which can be associated with the tumorigenic transformation. The levels of p53 is the same in the normal cells and in the tumorigenic derivative cells.